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Biomedical subjects

J B Brierley

Publications and source records attributed to J B Brierley.

16 recordsLinked to original sources
PubMed1979

Delayed pentobarbital administration limits ischemic brain damage in gerbils.

The capacity of delayed barbiturate administration to limit brain damage after unilateralcerebral ischemia was examined histologically in gerbils. The right common carotid artery was occluded in 50 animals under brief (3-minute) halothane anesthesia; 18 animals (36%) developed motor abnormalities consistent with stroke. The arterial clasps were removed after 1 hour and the abnormal animals were divided into treatment and placebo groups. Treated gerbils received sodium pentobarbital (70 mg/kg) intarperitoneally 1 hour after clasp removal and a smaller dose (50 mg/kg) 2 hours later; these animals lost corneal reflexes but retained spontaneous respiration and were kept normothermic. Animals in the placebo group received equivalent volumes of normal saline. Except for the period of anesthesia, both groups had similar postischemic motor behavior. Neuropathological examination of animals killed by perfusion-fixation after 24 hours revealed fewer pentobarbital-treated animals with shift of midline structures and with ipsilateral ischemic damage (including infarction). Compared with the placebo group, there was less extensive neuronal ischemic cell change in five regions of the ipsilateral cerebral hemispheres of the pentobarbital-treated animals (p less than 0.05). The results suggest that barbiturates administered as long as 1 hour after the end of an ischemic insult can still limit brain damage.

Animals↗
PubMed1979

Selective chromatolysis of neurons in the gerbil brain: a possible consequence of "epileptic" activity produced by common carotid artery occlusion.

Unilateral (50 to 118 minutes) and bilateral (2 to 33 minutes) carotid artery occlusion in gerbils resulted in two distinct types of neuronal alteration: ischemic cell change (ICC) in selectively vulnerable brain regions, and selective chromatolysis (SC) confined to the deeper layers of the cortex, the Sommer sector of zone h-1, and the paramedian region (PM) of the hippocampus. In typical SC the nucleus was eccentric and the Nissl substance was lost in the central eosinophilic cytoplasm. In electron micrographs this area of cytoplasm showed disruption of smooth and rough endoplasmic reticulum with disaggregation of polyribosomes and accumulation of mitochrondria and various dense bodies. SC was identified at 2 to 3 hours and was still recognizable at five days. When bilateral carotid artery occlusion lasted 5 to 6 minutes, SC was seen in the hippocampal Sommer sector and cerebral cortex, while ICC was restricted to the endfolium (h3-5). Unlike ICC, the frequency of SC was not related to the duration of ischemia but probably to the epileptic seizures (overt and subclinical) initiated by ischemia in the gerbil. These changes must be considered when the gerbil is employed as a model of experimental stroke.

Animals↗
PubMed1978

Profound hypoxia in Papio anubis and Macaca mulatta--physiological and neuropathological effects. I. Abrupt exposure following normoxia. II. Abrupt exposure following moderate hypoxia.

Lightly anaesthetized and spontaneously breathing P. anubis (PA) and M. mulatta (MM) inhaled at ambient pressure 3.2% oxygen (identical to 37,500 ft or 11,430 m) from air and also after pre-exposure to 14% oxygen (identical to 10,000 ft or 3,048 m). The EEG, ECG, respiratory rate, arterial and cerebral venous sinus pressures, end-tidal pO2 and pCO2 and body temperature were recorded. Arterial and cerebral venous sinus blood gases, pH and pyruvate and lactate contents were estimated. Before hypoxia, MM showed a relative hyperventilation. Profound hypoxia, from air, ended with the "last breath" at 89--205 sec in PA and at 93--570 sec in MM. Brain damage was restricted to one MM (4 exposures). Profound hypoxia after exposure to 14% oxygen ended with the "last breath" at 87--210 sec in PA and at 120 sec--94 min (including 9 exposures over 5 min) in MM. Brain damage was restricted to one MM ("last breath" at 94 min). In the two MM with brain damage there was evidence of reduction in cerebral perfusion near the end of profound hypoxia. Brain damage in one animal contrasts with the frequent and often severe brain damage in MM after equivalent sub-atmospheric decompressions preceded by exposure to moderate altitude (10,000 ft).

Animals↗
PubMed1978

E.E.G. monitoring for the control of anaesthesia produced by the infusion of althesin in primates.

The continuous infusion of Althesin under electroencephalographic (e.e.g.) control provided a constant level of light anaesthesia for periods of 1--5.5 h during experimental brain hypoxia in spontaneously breathing baboons and Rhesus monkeys. Polygraphic records (respiration, heart rate, arterial pressure, cerebral venous sinus pressure, end-tidal gas concentrations) and also estimation of blood-gas tensions, pH, and concentrations of pyruvate and lactate demonstrated a steady physiological state. Various methods of e.e.g. monitoring were tested to establish an optimal assessment of depth of anaesthesia as a guide to the control of the rate of infusion of Althesin. A purpose-built modification of the Cerebral Function Monitor was found to give unequivocal recognition of changing depths of anaesthesia.

Alfaxalone Alfadolone Mixture↗
PubMed1978

Epileptic brain damage: the role of systemic factors that modify cerebral energy metabolism.

The possible role of systemic physiological changes (occurring secondarily during status epilepticus) in the causation of epileptic brain damage has been evaluated in rats. Animals were anaesthetized, paralysed and mechanically ventilated; sustained electrocortical seizure discharges were induced by the intravenous injection of bicuculline, 1.2 mg/kg. After two hours of seizure activity brains were fixed by perfusion for histology. Physiological variables were maintained within certain limits from the end of the initial seizure phase (approximate duration twenty minutes) until two hours after onset of seizure to provide six groups: (1) Standard: mean arterial pressure above 120 mmHg, no hypoxia or hypoglycaemia, rectal temperature close to 37 degrees C. (2) Moderate Hypotension: mean arterial pressure at 70-75 mmHg. (3) Severe Hypotension: mean arterial pressure at 50 mmHg. (4) Hypoxia: arterial oxygen tension at 50 mmHg. (5) Hypoglycaemia: non-fed animals, with blood glucose close to 3.0 mumol/g. (6) Hyperthermia: rectal temperature at 40 degrees C. Microvacuolation and ischaemic cell change were identified by light microscopy in scattered neurons in the cortex (principally in the outer layers) in animals in three groups (Standard, Severe Hypotension and Hyperthermia). Similar neuronal changes were seen in the hippocampus (predominantly in the h1 or Sommer sector) in the Standard and Hyperthermia Groups. It is tentatively proposed that neuronal damage in animals with unrestricted cerebral oxygen and glucose availability is due to oxidative mechanisms in cells with excessively enhanced neuronal activity and that lesions caused by failing energy production do not appear until severe degrees of hypoxia are reached.

Animals↗
PubMed1977

Reversible profound depression of cerebral electrical activity in hyperthermia.

Transient major reduction of EEG activity in an hyperpyrexic patient (rectal temperature 42.5 degrees C) and transient isoelectric ECoG during accidental hyperthermia (rectal temperature 41.8 degrees C) in a Rhesus monkey are reported. Since recovery of electrocortical activity occurred in both instance this implies that in hyperthermia, as well as in hypothermia, an isoelectric EEG may not indicate irreversible brain damage.

Adult↗
PubMed1976

Cyanide intoxication in the rat: physiological and neuropathological aspects.

Sodium cyanide was given to rats by intravenous infusion at a rate that would avert apnoea (the first sign of overdosage) in the majority. There was full physiological monitoring in a group under anaesthesia and more limited monitoring in an unanaesthetized group. White matter was damaged in six animals and grey matter additionally in only one. It was concluded that cyanide can damage neurones only through the medium of secondary effects on circulation and respiration.

Animals↗
PubMed1975

Brief hypoxia-ischemia initially damages cerebral neurons.

Rats were studied during cerebral hypoxic ischemia to determine whether neurons or blood vessels suffered the first damage. Ten or more minutes of unilateral carotid artery occlusion combined with systemic hypoxemia (PaO-2, 21 mm Hg) produced neuronal but not vascular damage in the ipsilateral cerebral hemispheres of 18 of 29 rats (62%); two and five minute stresses caused no visible neuronal abnormalities. The longer exposures produced more widespread damage, and neuronal loss and gliomesodermal reaction were evident after prolonged survival. Early neuronal changes correlated with abnormalities of motor behavior (P less than .005). Despite neuronal damage that was sometimes extensive, vascular no-reflow developed in only one of 24 animals after 20 and 30 minutes of hypoxia-ischemia. Production of neuronal and neurological abnormalities in the absence of hypotension or vascular no-reflow indicates that hypoxia-ischemia initially damaged cerebral neurons.

Anesthesia, Inhalation↗
PubMed1975

Ischaemic brain damage in the gerbil in the absence of 'no-reflow'.

Approximately 40% of gerbils subjected to one hour of unilateral carotid artery occlusion displayed neurological abnormalities during that time. Most such animals were subsequently found to have ischaemic neuronal alterations within the territory of the ipsilateral middle cerebral artery. In contrast, impaired reperfusion ('no-reflow') rarely occurred and cannot therefore be implicated in the pathogenesis of ischaemic brain damage.

Animals↗
PubMedDate not supplied

Cyanide intoxication in Macaca mulatta. Physiological and neuropathological aspects.

Sodium cyanide was infused intravenously in 11 lightly anaesthetised and spontaneously breathing M. mulatta. In most, the EEG, ECG, respiratory rate, blood pressure, cerebral venous sinus pressure, end-tidal pCO2 and body temperature were recorded. Blood gases, pH, lactate and pyruvate were estimated in arterial and venous sinus blood samples. There was an initial hyperventilation with tetany in all animals. A rapid rate of cyanide infusion led to apnoea. An isoelectric or near-isoelectric EEG was usually precipitated by bradycardia often with additional hypotension. Neither epileptic seizures nor their EEG concomitants were seen at any stage. Three animals died of early heart failure. Brain damage was seen in 4 animals surviving up to 98 hr. White matter was involved in all. Ischaemic neuronal alterations, restricted to the striatum of one animal, were attributed to major circulatory complications. It was concluded that under these experimental conditions there is no evidence for hypoxic neuronal damage of purely histotoxic type.

Animals↗
PubMedDate not supplied

A new model of bilateral hemispheric ischemia in the unanesthetized rat.

A new model of transient, bilateral hemispheric ischemia in the unanesthetized rat is described. During ether anesthesia the rat's vertebral arteries were electrocauterized through the alar foramina of the first cervical vertebra and reversible clasps placed loosely around the common carotid arteries. Twenty-four hr later, the awake rats were restrained and the carotid clasps tightened to produce 4-vessel occlusion. The carotid clasps were removed after 10, 20 or 30 min of 4-vessel occlusion and the animals killed by perfusion fixation 72 hr later. Rats which convulsed during the ischemic or post-ischemic period were excluded from further study. All rats subjected to 20 or 30 min of 4-vessel occlusion demonstrated ischemic neuronal damage. The H1 and paramedian hippocampus, striatum and layers 3, 5 and 6 of the posterior neocortex were the regions most frequently damaged. The advantages of this model are the ease of preparation of large numbers of animals, a high rate of predictable ischemic neuronal damage, a low incidence of seizures and the absence of anesthesia.

Animals↗